The aim of the present study was to determine whether the effects and underlying mechanisms of ticagrelor in a rat model of sepsis-induced acute kidney injury (AKI) were mediated via the CD62P pathway. A total of 15 rats were randomly assigned to the following groups: Normal, sham, cecal ligation and puncture (CLP), CLP + clinical dose of ticagrelor (CCD) and CLP + loading dose of ticagrelor (CLD). Ticagrelor was administered 12 h before modeling, immediately after modeling, and 12 h after modeling at a dose of 8.6 and 46.42 mg/kg in the CCD and CLD groups, respectively. Rats in the normal, sham and CLP groups were treated with the same volume of distilled water. Serum creatinine (SCr), CD62P and interleukin-1β (IL-1β) levels, myeloperoxidase (MPO) activity in the renal tissue and the apoptosis rate of renal cells were increased in the CLP group, compared with in the normal and sham groups (P<0.05). In addition, ticagrelor treatment reduced SCr, CD62P and IL-1β expression levels, renal tissue MPO activity and renal cell apoptosis in rats with sepsis-induced AKI (P<0.05). CD62P expression was closely associated with the occurrence of sepsis-induced AKI. The mechanism of ticagrelor-mediated reductions in inflammation, renal neutrophil infiltration and renal cell apoptosis is possibly associated with reductions in CD62P expression.
Keywords: CD62P; acute kidney injury; apoptosis; inflammation; sepsis; ticagrelor.
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